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Environmental Pollution (Barking, Essex... Mar 2024Leather is produced by a multi-step process among which the tanning phase is the most relevant, transforming animal skin collagen into a stable, non-putrescible material... (Review)
Review
Leather is produced by a multi-step process among which the tanning phase is the most relevant, transforming animal skin collagen into a stable, non-putrescible material used to produce a variety of different goods, for the footwear, automotive, garments, and sports industry. Most of the leather produced today is tanned with chromium (III) salts or alternatively with aldehydes or synthetic tannins, generating high environmental concern. Over the years, high exhaustion tanning systems have been developed to reduce the environmental impact of chromium salts, which nevertheless do not avoid the use of metals. Chrome-free alternatives such as aldehydes and phenol based synthetic tannins, are suffering from Reach restrictions due to their toxicity. Thus, the need for environmentally benign and economically sustainable tanning agents is increasingly urgent. In this review, the synthesis, use and tanning mechanism of a new class of tanning agents, 1,3,5-triazines derivatives, have been reported together with organoleptic, physical mechanical characteristics of tanned leather produced. Additionally environmental performance and economic data available for 1,3,5-triazines have been compared with those of a standard basic chromium sulphate tanning process, evidencing the high potentiality for sustainable, metal, aldehyde, and phenol free leather manufacturing.
Topics: Animals; Aldehydes; Chromium; Industrial Waste; Industry; Phenol; Phenols; Salts; Tanning; Tannins; Triazines
PubMed: 38320686
DOI: 10.1016/j.envpol.2024.123472 -
Journal of Advanced Research Feb 2024It has been shown that polystyrenenanoplastic (PS-NP) exposure induces toxicity in the lungs.
INTRODUCTION
It has been shown that polystyrenenanoplastic (PS-NP) exposure induces toxicity in the lungs.
OBJECTIVES
This study aims to provide foundational evidence to corroborate that ferroptosis and abnormal HIF-1α activity are the main factors contributing to pulmonary dysfunction induced by PS-NP exposure.
METHODS
Fifty male and female C57BL/6 mice were exposed to distilled water or 100 nm or 200 nm PS-NPs via intratracheal instillation for 7 consecutive days. Hematoxylin and eosin (H&E) and Masson trichrome staining were performed to observe the histomorphological changes in the lungs. To clarify the mechanisms of PS-NP-induced lung injury, we used 100 μg/ml, 200 μg/ml and 400 μg/ml 100 or 200 nm PS-NPs to treat the human lung bronchial epithelial cell line BEAS-2B for 24 h. RNA sequencing (RNA-seq) of BEAS-2B cells was performed following exposure. The levels of glutathione, malondialdehyde, ferrous iron (Fe), and reactive oxygen species (ROS) were measured. The expression levels of ferroptotic proteins were detected in BEAS-2B cells and lung tissues by Western blotting. Western blotting, immunohistochemistry, and immunofluorescence were used to evaluate the HIF-1α/HO-1 signaling pathway activity.
RESULTS
H&E staining revealed substantial perivascular lymphocytic inflammation in a bronchiolocentric pattern, and Masson trichrome staining demonstrated critical collagen deposits in the lungs after PS-NP exposure. RNA-seq revealed that the differentially expressed genes in PS-NP-exposed BEAS-2B cells were enriched in lipid metabolism and iron ion binding processes. After PS-NP exposure, the levels of malondialdehyde, Fe, and ROS were increased, but glutathione level was decreased. The expression levels of ferroptotic proteins were altered significantly. These results verified that PS-NP exposure led to pulmonary injury through ferroptosis. Finally, we discovered that the HIF-1α/HO-1 signaling pathway played an important role in regulating ferroptosis in the PS-NP-exposed lung injury.
CONCLUSION
PS-NP exposure caused ferroptosis in bronchial epithelial cells by activating the HIF-1α/HO-1 signaling pathway, and eventually led to lung injury.
Topics: Mice; Humans; Animals; Female; Male; Mice, Inbred C57BL; Lung Injury; Ferroptosis; Reactive Oxygen Species; Bronchi; Eosine Yellowish-(YS); Glutathione; Iron; Malondialdehyde
PubMed: 36933884
DOI: 10.1016/j.jare.2023.03.003 -
Microbial Cell Factories Aug 2023Vanillin (4-hydroxy-3-methoxybenzaldehyde) is one of the most popular flavors with wide applications in food, fragrance, and pharmaceutical industries. However, the high... (Review)
Review
Vanillin (4-hydroxy-3-methoxybenzaldehyde) is one of the most popular flavors with wide applications in food, fragrance, and pharmaceutical industries. However, the high cost and limited yield of plant extraction failed to meet the vast market demand of natural vanillin. Vanillin biotechnology has emerged as a sustainable and cost-effective alternative to supply vanillin. In this review, we explored recent advances in vanillin biosynthesis and highlighted the potential of vanillin biotechnology. In particular, we addressed key challenges in using microorganisms and provided promising approaches for improving vanillin production with a special focus on chassis development, pathway construction and process optimization. Future directions of vanillin biosynthesis using inexpensive precursors are also thoroughly discussed.
Topics: Biotechnology; Benzaldehydes
PubMed: 37543600
DOI: 10.1186/s12934-023-02144-9 -
Drug Delivery and Translational Research Sep 2023Diabetic wounds are a serious complication of diabetes mellitus (DM) that can lead to persistent infection, amputation, and even death. Prolonged oxidative stress has...
Diabetic wounds are a serious complication of diabetes mellitus (DM) that can lead to persistent infection, amputation, and even death. Prolonged oxidative stress has been widely recognized as a major instigator in the development of diabetic wounds; therefore, oxidative stress is considered a promising therapeutic target. In the present study, Keap1/Nrf2 signaling was confirmed to be activated in streptozotocin (STZ)-induced diabetic mice and methylglyoxal (MGO)-treated human umbilical vein endothelial cells (HUVECs). Knockdown of Keap1 by siRNA reversed the increase in Keap1 levels, promoted the nuclear translocation of Nrf2, and increased the expression of HO-1, an antioxidant protein. To explore therapeutic delivery strategies, milk-derived exosomes (mEXOs) were developed as a novel, efficient, and non-toxic siRNA carrier. SiRNA-Keap1 (siKeap1) was loaded into mEXOs by sonication, and the obtained mEXOs-siKeap1 were found to promote HUVEC proliferation and migration while relieving oxidative stress in MGO-treated HUVECs. Meanwhile, in a mouse model of diabetic wounds, injection of mEXOs-siKeap1 significantly accelerated diabetic wound healing with enhanced collagen formation and neovascularization. Taken together, these data support the development of Keap1 knockdown as a potential therapeutic strategy for diabetic wounds and demonstrated the feasibility of mEXOs as a scalable, biocompatible, and cost-effective siRNA delivery system. The therapeutic effect of siKeap1-loaded mEXOs on diabetic wound healing was assessed. First, we found that the expression of Keap1 was upregulated in the wounds of diabetic mice and in human umbilical vein endothelial cells (HUVECs) pretreated with methylglyoxal (MGO). Next, we extracted exosomes from raw milk by differential centrifugation and loaded siKeap1 into milk-derived exosomes by sonication. The in vitro application of the synthetic complex (mEXOs-siKeap1) was found to increase the nuclear localization of Nrf2 and the expression of the antioxidant protein HO-1, thus reversing oxidative stress. Furthermore, in vivo mEXOs-siKeap1 administration significantly accelerated the healing rate of diabetic wounds (Scheme 1). Scheme 1 Schematic diagram. A Synthesis of mEXOs-siKeap1 complex. B Mechanism of mEXOs-siKeap1 in vitro. C The treatment effect of mEXOs-siKeap1 on an in vivo mouse model of diabetic wounds.
Topics: Mice; Humans; Animals; Antioxidants; Kelch-Like ECH-Associated Protein 1; Diabetes Mellitus, Experimental; RNA, Small Interfering; Milk; Exosomes; NF-E2-Related Factor 2; Magnesium Oxide; Pyruvaldehyde; Wound Healing; Oxidative Stress; Human Umbilical Vein Endothelial Cells
PubMed: 36749479
DOI: 10.1007/s13346-023-01306-x -
Journal of Cachexia, Sarcopenia and... Aug 2023Muscle wasting during cancer cachexia is mediated by protein degradation via autophagy and ubiquitin-linked proteolysis. These processes are sensitive to changes in...
BACKGROUND
Muscle wasting during cancer cachexia is mediated by protein degradation via autophagy and ubiquitin-linked proteolysis. These processes are sensitive to changes in intracellular pH ([pH] ) and reactive oxygen species, which in skeletal muscle are partly regulated by histidyl dipeptides, such as carnosine. These dipeptides, synthesized by the enzyme carnosine synthase (CARNS), remove lipid peroxidation-derived aldehydes, and buffer [pH] . Nevertheless, their role in muscle wasting has not been studied.
METHODS
Histidyl dipeptides in the rectus abdominis (RA) muscle and red blood cells (RBCs) of male and female controls (n = 37), weight stable (WS: n = 35), and weight losing (WL; n = 30) upper gastrointestinal cancer (UGIC) patients, were profiled by LC-MS/MS. Expression of enzymes and amino acid transporters, involved in carnosine homeostasis, was measured by Western blotting and RT-PCR. Skeletal muscle myotubes were treated with Lewis lung carcinoma conditioned medium (LLC CM), and β-alanine to study the effects of enhancing carnosine production on muscle wasting.
RESULTS
Carnosine was the predominant dipeptide present in the RA muscle. In controls, carnosine levels were higher in men (7.87 ± 1.98 nmol/mg tissue) compared with women (4.73 ± 1.26 nmol/mg tissue; P = 0.002). In men, carnosine was significantly reduced in both the WS (5.92 ± 2.04 nmol/mg tissue, P = 0.009) and WL (6.15 ± 1.90 nmol/mg tissue; P = 0.030) UGIC patients, compared with controls. In women, carnosine was decreased in the WL UGIC (3.42 ± 1.33 nmol/mg tissue; P = 0.050), compared with WS UGIC patients (4.58 ± 1.57 nmol/mg tissue), and controls (P = 0.025). Carnosine was significantly reduced in the combined WL UGIC patients (5.12 ± 2.15 nmol/mg tissue) compared with controls (6.21 ± 2.24 nmol/mg tissue; P = 0.045). Carnosine was also significantly reduced in the RBCs of WL UGIC patients (0.32 ± 0.24 pmol/mg protein), compared with controls (0.49 ± 0.31 pmol/mg protein, P = 0.037) and WS UGIC patients (0.51 ± 0.40 pmol/mg protein, P = 0.042). Depletion of carnosine diminished the aldehyde-removing ability in the muscle of WL UGIC patients. Carnosine levels were positively associated with decreases in skeletal muscle index in the WL UGIC patients. CARNS expression was decreased in the muscle of WL UGIC patients and myotubes treated with LLC-CM. Treatment with β-alanine, a carnosine precursor, enhanced endogenous carnosine production and decreased ubiquitin-linked protein degradation in LLC-CM treated myotubes.
CONCLUSIONS
Depletion of carnosine could contribute to muscle wasting in cancer patients by lowering the aldehyde quenching abilities. Synthesis of carnosine by CARNS in myotubes is particularly affected by tumour derived factors and could contribute to carnosine depletion in WL UGIC patients. Increasing carnosine in skeletal muscle may be an effective therapeutic intervention to prevent muscle wasting in cancer patients.
Topics: Female; Humans; Male; Aldehydes; beta-Alanine; Carcinoma, Lewis Lung; Carnosine; Chromatography, Liquid; Dipeptides; Muscle, Skeletal; Muscular Atrophy; Tandem Mass Spectrometry; Ubiquitins
PubMed: 37199284
DOI: 10.1002/jcsm.13258 -
Frontiers in Immunology 2023Mucosal-associated invariant T (MAIT) cells are a population of innate-like T cells, which mediate host immunity to microbial infection by recognizing metabolite...
INTRODUCTION
Mucosal-associated invariant T (MAIT) cells are a population of innate-like T cells, which mediate host immunity to microbial infection by recognizing metabolite antigens derived from microbial riboflavin synthesis presented by the MHC-I-related protein 1 (MR1). Namely, the potent MAIT cell antigens, 5-(2-oxopropylideneamino)-6-D-ribitylaminouracil (5-OP-RU) and 5-(2-oxoethylideneamino)-6-D-ribitylaminouracil (5-OE-RU), form via the condensation of the riboflavin precursor 5-amino-6-D-ribitylaminouracil (5-A-RU) with the reactive carbonyl species (RCS) methylglyoxal (MG) and glyoxal (G), respectively. Although MAIT cells are abundant in humans, they are rare in mice, and increasing their abundance using expansion protocols with antigen and adjuvant has been shown to facilitate their study in mouse models of infection and disease.
METHODS
Here, we outline three methods to increase the abundance of MAIT cells in C57BL/6 mice using a combination of inflammatory stimuli, 5-A-RU and MG.
RESULTS
Our data demonstrate that the administration of synthetic 5-A-RU in combination with one of three different inflammatory stimuli is sufficient to increase the frequency and absolute numbers of MAIT cells in C57BL/6 mice. The resultant boosted MAIT cells are functional and can provide protection against a lethal infection of .
CONCLUSION
These results provide alternative methods for expanding MAIT cells with high doses of commercially available 5-A-RU (± MG) in the presence of various danger signals.
Topics: Humans; Animals; Mice; Mice, Inbred C57BL; Mucosal-Associated Invariant T Cells; Adjuvants, Immunologic; Pyruvaldehyde; Riboflavin
PubMed: 37720229
DOI: 10.3389/fimmu.2023.1109759 -
Redox Biology Jul 2023Psoriasis, one of the most frequent immune-mediated skin diseases, is manifested by numerous psoriatic lessons on the skin caused by excessive proliferation and... (Review)
Review
Psoriasis, one of the most frequent immune-mediated skin diseases, is manifested by numerous psoriatic lessons on the skin caused by excessive proliferation and keratinization of epidermal cells. These disorders of keratinocyte metabolism are caused by a pathological interaction with the cells of the immune system, including lymphocytes, which in psoriasis are also responsible for systemic inflammation. This is accompanied by oxidative stress, which promotes the formation of lipid peroxidation products, including reactive aldehydes and isoprostanes, which are additional pro-inflammatory signaling molecules. Therefore, the presented review is focused on highlighting changes that occur during psoriasis development at the level of lipid peroxidation products, including 4-hydroxynonenal, 4-oxononenal, malondialdehyde, and acrolein, and their influence on protein structures. Furthermore, we will examine inducing agents of cellular functioning, as well as intercellular signaling. These lipid peroxidation products can form adducts with a variety of proteins with different functions in the body, including proteins within skin cells and cells of the immune system. This is especially true in autoimmune diseases such as psoriasis. For example, these changes concern proteins involved in maintaining redox homeostasis or pro-inflammatory signaling. Therefore, the formation of such adducts should attract attention, especially during the design of preventive cosmetics or anti-psoriasis therapies.
Topics: Humans; Lipid Peroxidation; Aldehydes; Malondialdehyde; Psoriasis; Proteins; Oxidation-Reduction
PubMed: 37150149
DOI: 10.1016/j.redox.2023.102729 -
Free Radical Biology & Medicine Feb 2024Autophagy, which is responsible for removing damaged molecules, prevents their accumulation in cells, thus maintaining intracellular homeostasis. It is also responsible... (Review)
Review
Autophagy, which is responsible for removing damaged molecules, prevents their accumulation in cells, thus maintaining intracellular homeostasis. It is also responsible for removing the effects of oxidative stress, so its activation takes place during increased reactive oxygen species (ROS) generation and lipid peroxidation. Therefore, the aim of this review was to summarize all the available knowledge about the effect of protein modifications by lipid peroxidation products on autophagy activation and the impact of this interaction on the functioning of cells. This review shows that reactive aldehydes (including 4-hydroxynonenal and malondialdehyde), either directly or by the formation of adducts with autophagic proteins, can activate or prevent autophagy, depending on their concentration. This effect relates not only to the initial stages of autophagy, when 4-hydroxynonenal and malondialdehyde affect the levels of proteins involved in autophagy initiation and phagophore formation, but also to the final stage, degradation, when reactive aldehydes, by binding to the active center of cathepsins, inactivate their proteolytic functions. Moreover, this review also shows how little research exists on analyzing the impact of lipid peroxidation products and their protein adducts on autophagy. Such knowledge could be used in the therapy of diseases related to autophagy disorders.
Topics: Lipid Peroxidation; Aldehydes; Malondialdehyde; Autophagy; Oxidative Stress; Proteins
PubMed: 38182071
DOI: 10.1016/j.freeradbiomed.2024.01.001 -
Molecular Medicine Reports Nov 2023The alteration of metabolism is essential for the initiation and progression of numerous types of cancer, including colorectal cancer (CRC). Metabolomics has been used...
The alteration of metabolism is essential for the initiation and progression of numerous types of cancer, including colorectal cancer (CRC). Metabolomics has been used to study CRC. At present, the reprogramming of the metabolism in CRC remains to be fully elucidated. In the present study, comprehensive untargeted metabolomics analysis was performed on the paired CRC tissues and adjacent normal tissues from patients with CRC (n=35) using ultra‑high‑performance liquid chromatography‑mass spectrometry. Subsequently, bioinformatic analysis was performed on the differentially expressed metabolites. The changes in these differential metabolites were compared among groups of patients based on sex, anatomical tumor location, grade of tumor differentiation and stage of disease. A total of 927 metabolites were detected in the tissue samples, and 24 metabolites in the CRC tissue were significantly different compared with the adjacent normal tissue. The present study revealed that the levels of three amino acid metabolites were increased in the CRC tissue, specifically, N‑α‑acetyl‑ε‑(2‑propenal)‑Lys, cyclo(Glu‑Glu) and cyclo(Phe‑Glu). The metabolites with decreased levels in the CRC tissue included quinaldic acid (also referred to as quinoline‑2‑carboxilic acid), 17α‑ and 17β‑estradiol, which are associated with tumor suppression activities, as well as other metabolites such as, anhydro‑β‑glucose, Asp‑Arg, lysophosphatidylcholine, lysophosphatidylethanolamine (lysoPE), lysophosphatidylinositol, carnitine, 5'‑deoxy‑5'‑(methylthio) adenosine, 2'‑deoxyinosine‑5'‑monophosphate and thiamine monophosphate. There was no difference in the levels of the differential metabolites between male and female patients. The differentiation of CRC also showed no impact on the levels of the differential metabolites. The levels of lysoPE were increased in the right side of the colon compared with the left side of the colon and rectum. Analysis of the different tumor stages indicated that 2‑aminobenzenesulfonic acid, P‑sulfanilic acid and quinoline‑4‑carboxylic acid were decreased in stage I CRC tissue compared with stage II, III and IV CRC tissue. The levels of N‑α‑acetyl‑ε‑(2‑propenal)‑Lys, methylcysteine and 5'‑deoxy‑5'‑(methylthio) adenosine varied at different stages of tumorigenesis. These differential metabolites were implicated in multiple metabolism pathways, including carbohydrate, amino acid, lipid, nucleotide and hormone. In conclusion, the present study demonstrated that CRC tumors had altered metabolites compared with normal tissue. The data from the metabolic profile of CRC tissues in the present study provided supportive evidence to understand tumorigenesis.
Topics: Humans; Male; Female; Acrolein; Metabolomics; Colorectal Neoplasms; Amino Acids; Carcinogenesis
PubMed: 37772396
DOI: 10.3892/mmr.2023.13106 -
Methylglyoxal, a highly reactive dicarbonyl compound, as a threat for blood brain barrier integrity.Fluids and Barriers of the CNS Oct 2023The brain is a highly metabolically active organ requiring a large amount of glucose. Methylglyoxal (MGO), a by-product of glucose metabolism, is known to be involved in... (Review)
Review
The brain is a highly metabolically active organ requiring a large amount of glucose. Methylglyoxal (MGO), a by-product of glucose metabolism, is known to be involved in microvascular dysfunction and is associated with reduced cognitive function. Maintenance of the blood-brain barrier (BBB) is essential to maintain optimal brain function and a large amount of evidence indicates negative effects of MGO on BBB integrity. In this review, we summarized the current literature on the effect of MGO on the different cell types forming the BBB. BBB damage by MGO most likely occurs in brain endothelial cells and mural cells, while astrocytes are most resistant to MGO. Microglia on the other hand appear to be not directly influenced by MGO but rather produce MGO upon activation. Although there is clear evidence that MGO affects components of the BBB, the impact of MGO on the BBB as a multicellular system warrants further investigation. Diminishing MGO stress can potentially form the basis for new treatment strategies for maintaining optimal brain function.
Topics: Blood-Brain Barrier; Endothelial Cells; Pyruvaldehyde; Magnesium Oxide; Brain
PubMed: 37875994
DOI: 10.1186/s12987-023-00477-6